## Cytokine Profile in Allergic Nasal Polyps **Key Point:** Interleukin-5 (IL-5) is the primary Th2 cytokine driving eosinophil differentiation, recruitment, and survival in allergic nasal polyps. ### IL-5 Mechanism in Nasal Polyp Pathogenesis 1. **Th2 cell activation** → IL-5 production 2. **Bone marrow eosinophil precursor proliferation** → IL-5 receptor signaling 3. **Eosinophil migration** to nasal mucosa via chemokine gradients (eotaxin, CCL11) 4. **Eosinophil survival and activation** → tissue damage via cationic proteins **High-Yield:** IL-5 is the central axis of allergic inflammation in nasal polyps; monoclonal anti-IL-5 antibodies (mepolizumab) are now approved for severe eosinophilic nasal polyposis. ### Cytokine Roles in Nasal Polyp Inflammation | Cytokine | Source | Function | Relevance to Polyps | |---|---|---|---| | IL-5 | Th2 cells, mast cells | Eosinophil recruitment & survival | **Primary driver** | | IL-4 | Th2 cells | IgE class switching, Th2 polarization | Supporting role | | Eotaxin (CCL11) | Epithelial cells, fibroblasts | Eosinophil chemotaxis | Co-mediator with IL-5 | | IFN-γ | Th1 cells | Th1 response, macrophage activation | Absent/low in allergic polyps | | TNF-α | Macrophages, mast cells | General inflammation | Non-specific | **Clinical Pearl:** Patients with nasal polyps often have elevated serum IgE and tissue eosinophilia, reflecting a Th2-dominant immune response. Blocking IL-5 reduces polyp size and symptom burden in eosinophilic nasal polyposis. **Mnemonic:** **EASI** = Eosinophils, Allergic inflammation, Severe polyps, IL-5 is the key. [cite:Harrison 21e Ch 335] 
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